Kinetic Analysis of Agonist-Induced Down-Regulation of the β2-Adrenergic Receptor in BEAS-2B Cells Reveals High- and Low-Affinity Components

2000 ◽  
Vol 58 (2) ◽  
pp. 421-430 ◽  
Author(s):  
Bruce R. Williams ◽  
Roger Barber ◽  
Richard B. Clark
Keyword(s):  
Kinetic Analysis ◽  
Adrenergic Receptor ◽  
Down Regulation ◽  
Β2 Adrenergic Receptor

scholarly journals β2-Adrenergic Receptor Down-regulation

1999 ◽  
Vol 274 (41) ◽  
pp. 28900-28908 ◽  
Author(s):  
Ralf Jockers ◽  
Stéphane Angers ◽  
Angelo Da Silva ◽  
Philippe Benaroch ◽  
A. Donny Strosberg ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Down Regulation ◽  
Β2 Adrenergic Receptor

scholarly journals Centella Asiatica (GOTU KOLA) TREATMENT ATTENUATES PRO-INFLAMMATORY MEDIATORS IN LIVER OF RATS WITH ELECTRICAL FOOT SHOCK STRESS MODEL

2020 ◽  
Vol 17 (2) ◽  
pp. 1-7
Author(s):  
Dwi Cahyani Ratna Sari ◽  
Wiwit Ananda Wahyu Setyaningsih ◽  
Rizky Nur Mainichi ◽  
Gita Mumtarin Dara ◽  
Ratih Kemalasari ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Adrenergic Receptor ◽  
Centella Asiatica ◽  
Control Group ◽  
Stress Model ◽  
Down Regulation ◽  
Stress Group ◽  
Tnf Α ◽  
Β2 Adrenergic Receptor ◽  
Shock Stress

Background: Stress induces secretion of cathecolamines and glucocorticoids, which may produce liver injury. Followed by the production of inflammatory mediators, it causes apoptosis. Centella asiatica (CeA) has anti-inflammatory and hepatoprotective effects. The present study aims to determine the role of CeA in the attenuation of liver pro-inflammatory mediator expression in rats with electrical foot shock stress model. Materials and Methods: Twenty-four Sprague-Dawley rats were randomized into four groups consisted of six rats each: (1) Control group, (2) CeA-treated group, (3) Stress group, and (4) CeA + stress group. Reverse transcriptase PCR of inflammatory and apoptosis markers as well as Real-Time PCR of β2-adrenergic receptor were performed from liver tissues. Results: Electrical foot shock stress induced up-regulation of NFκB and TNF-α mRNA expressions as pro-inflammatory mediators, compared to control group. This alteration was followed by up-regulation of BAX and β2-adrenergic receptor, as well as the down-regulation of BCl2 compared to control. CeA treatment prevented enhancement of NFκB, TNF-α, TLR-4 and β-adrenergic receptor mRNA expressions, which was followed by down-regulation of BAX and up-regulation of BCl-2, compared to stress group. Conclusion: CeA prevents secretion of pro-inflammatory chemokines and cytokines as well as apoptotic markers in liver cells through the activation of β2-adrenergic receptor.

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